Transvascular pulmonary fluid transport can be altered by either changing the permeability-surface area (PS) of the exchange barrier or by changing the overall plasma to interstitial fluid driving force. I am currently investigating the effects of altering either the driving force or capillary surface area on net fluid movement in the lung. Experiments are underway in which pulmonary microvascular pressure is elevated in stages by inflating a balloon in the left atrium of unanesthetized sheep. The following parameters are measured: pulmonary artery pressure, left atrial pressure, plasma and lymph colloid osmotic pressure and concentration, the concentrations of eight plasma and lymph protein fractions, lung lymph flow, blood gases, cardiac output and tracer estimates of water PS, urea PS, and extravascular lung water. Future experiments will probe the effects of isotonic volume loading, hypotonic and hypertonic protein infusions, and increased or decreased body temperature on transvascular fluid and protein exchange. A mathematical model, based on an equivalent pore analog of the capillary barrier, will be applied to the data. The model-predicted interstitial water volume and lymph protein concentrations are being compared with measured values throughout the transient period. If agreement with experimental data is good the model will be used to predict conditions which may leas to lung edema and, in addition, can be used to predict the rate at which water accumulates in the lungs.